Congestive Heart Failure (CHF) is one of the major causes of death in the United States. CHF severely affects an estimated two million people in the United States and causes approximately 400,000 deaths per year. CHF is also one of the most significant burdens on health care costs. It is estimated that the costs to Medicare for the treatment of CHF is about $40 billion each year.
Current treatments for CHF include pharmaceuticals such as ACE inhibitors, Angiotensin II receptor blocker, and beta blockers. These pharmaceuticals have only moderately reduced mortality rates, however. Additionally they pose risks of adverse drug reactions or interactions.
Invasive therapies such as implantable defibrillators and dual chamber, cardiac “resynchronization” pacemakers are also utilized to manage CHF patients whose hearts have a rhythm abnormality, about 30% of CHF patients. These therapies are extremely expensive (implantation of such devices in the U.S. currently costs $50,000 or more), require surgery and have shown only a reduction in mortality of about 50% from the American Heart Association's published figure of 18.8% annual mortality from CHF in the United States.
External counterpulsation (ECP) is currently gaining acceptance as an effective therapy for angina and CHF. “Counter Pulsation” decreases cardiac workload and improves heart function by increasing blood flow through the coronary vessels using a series of cuffs, fastened about the legs and buttocks, which contain inflatable bladders. “External” means that the treatment is applied to the exterior of the of the patient's body and is non-invasive. Surgery, anesthesia and injections are not required.
ECP is a safe and effective treatment to assist circulation, particularly in the treatment of ischemic heart disease. It has also been shown to increase diastolic pressure and flow through the coronary arteries, cause angiogenesis by the release of naturally occurring angiogenic growth factors, reduce systolic pressure and the work effort of the heart, induce endothelial remodeling, improve vessel elasticity, produce neurohormonal benefits and release nitrous oxide, a potent vasodilator.
The ECP treatment system compresses the legs from the calves through the thighs, and the buttocks, by sequentially inflating sets of bladders encased in flexible, fabric cuffs during the resting phase of the heart cycle (diastole). This results in the movement of blood from the legs and buttocks toward the heart through both the arterial and the venous systems.
Each wave of pressure is electronically timed to the patient's electrocardiogram (ECG) so that blood flow to the heart is increased during the time period the heart is relaxing (diastole). Before the heart begins to contract again (systole), the pressure is rapidly released. This lowers resistance in the blood vessels of the legs and the buttocks, enabling blood to be pumped more easily from the heart, decreasing the amount of work required of the heart muscle. Also, blood forced up the veins by ECP returns to the heart and is termed “pre-loading” the heart. These effects are evidenced by a reduction in the patient's systolic pressure.
The aortic valve is the heart valve through which blood leaves the left ventricle, the main pumping chamber of the heart, and which prevents back flow into the left ventricle. During diastole, the aortic valve is closed. The coronary arteries open off the aorta, above the aortic valve, and the pressure applied to the lower extremities drives blood up the arteries into the aorta and, since the aortic valve is closed, the blood exits the aorta through the coronary arteries, expanding the heart's networks of tiny auxiliary blood vessels called “collaterals”. This is evidenced by an increase in the patient's diastolic pressure. The volume of blood flowing to the heart muscle is thus increased.
The typical ECP treatment regimen for chronic angina patients whose left ventricular ejection fraction (LVEF) is normal (50% to 70%) is 35 hours of treatment, usually one-hour per day, five days per week for seven weeks. Alternatively, ECP may be applied for one-hour per day, six days a week for six weeks, a total of 36 hours. While not as desirable as the above-regimens, a 2-hour per day regimen can also be utilized, which reduces the time to completion to 3 or 3½ weeks.
Pressure is typically applied to produce a peak diastolic pressure to peak systolic pressure ratio (D/S Ratio) of 1.5:1 to 2:1 or higher in the treatment of such chronic angina patients. The duration of treatment and rest intervals depend on the patient's condition, the degree of augmentation of diastolic pressure to systolic pressure obtained, the patient's LVEF, patient tolerance to ECP and like indications.
Currently practiced ECP methods, such as those used in the treatment of chronic angina with substantially normal LVEF (i.e., at D/S Ratio of 1.5:1 to 2:1 or higher), can cause excessive pre-loading of the heart. If the patient also suffers from CHF and exhibits a LVEF less than 50%, the heart cannot pump out or “eject” a sufficient amount of blood. This causes blood to “pool” or build up in the blood vessels of the lungs, abdomen and extremities, as well as fluid to build-up in the calves, ankles and feet. The heart muscle necessarily works harder and thickens, which further reduces its pumping efficiency. As a result, more fluid builds up in the lungs, making it difficult for the patient to breathe. A recurrence or worsening of heart failure or even death can result.
The ECP therapy method disclosed herein seeks to use a graduated series of steps, in which the D/S Ratio is periodically increased, starting at a relatively low pressure to avoid the undesirable consequences of the currently practiced high pressure ECP regimen therapy for angina. This graduated low pressure ECP regimen can benefit CHF and heart attack patients, as well as those with other conditions that cause a low LVEF such as ischemic strokes, acute renal or hepatic failure, cardiogenic shock, and the like. Such graduated low pressure ECP regimen therapy leads to a substantial long-term reduction in hospitalization and mortality, as well as an improvement in the condition and quality of life of the patient.
The method disclosed herein also seeks to include a group of patients that are excluded from the current high pressure ECP Regimen therapy for angina; patients with low LVEF.
There is thus a need for a non-invasive means to effectively treat and manage patients with CHF and other ailments exhibiting a decrease in the volume of blood flow the heart can eject on such compression, such as the ECP Regimen therapy disclosed herein.